Figure 2.

Scheme: Putative pathophysiological role(s) of cardiac A_2A-ARs. A_2A-ARs can enhance LPS via receptors in the sarcolemmal alters nuclear gene transcription and putative detrimental proteins are made that impair cardiac contractility. Hypoxia and ischemia impair respiration and thus ATP formation in mitochondria or activate directly hypoxia dependent transcription factors. The mitochondrial process is attenuated by compounds like 5-hydroxy-deanoate (5-HD). Adriamycin impairs mitochondrial function. Hypertension can lead to hypertrophy which alters cardiac gene expression in detrimental ways leading to arrhythmias and heart failure. Altered expression of sarcolemmal ion channels and stimulation of A_2A-ARs can lead to supraventricular or ventricular arrhythmias by alteration of Ca²⁺ homeostasis.